Protective effect of a mitochondria-targeting peptide against paclitaxel-induced peripheral neuropathy

被引:3
|
作者
Itoh, Kensaku [1 ]
Shimoyama, Megumi [1 ]
Schiller, Peter W. [2 ,3 ]
Toyama, Satoshi [1 ,4 ,5 ]
机构
[1] Jikei Univ, Ctr Neurosci Pain, Sch Med, Tokyo, Japan
[2] Montreal Clin Res Inst, Lab Chem Biol & Peptide Res, Montreal, PQ, Canada
[3] Univ Montreal, Dept Pharmacol & Physiol, Montreal, PQ, Canada
[4] Tokyo Med & Dent Univ, Grad Sch Med & Dent Sci, Dept Anesthesiol, Tokyo, Japan
[5] Jikei Univ, Ctr Neurosci Pain, Sch Med, 3 25 8 Nishi Shimbashi,Minato ku, Tokyo 1058471, Japan
基金
加拿大健康研究院; 日本学术振兴会; 美国国家卫生研究院;
关键词
neuropathic; painchemotherapy; chemotherapy-induced peripheral neuropathy; mitochondria; paclitaxel; pain; RAT; OXALIPLATIN; PAIN;
D O I
10.1111/cbdd.14192
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Chemotherapy-induced peripheral neuropathy (CIPN) is a major side effect of several anticancer agents including paclitaxel, a chemotherapeutic drug widely used in cancer treatment. CIPN deteriorates patients' quality of life and compromises cancer treatment. Dysfunction or injury of mitochondria has been suggested to be involved in the induction of this neuropathy. SS-20 is a tetrapeptide that targets mitochondria and restores mitochondrial bioenergetics. This study was aimed to examine the protective effect of SS-20 against paclitaxel-induced peripheral neuropathy using a murine model. Repeated administration of paclitaxel to mice induced peripheral neuropathy as demonstrated by the presence of mechanical allodynia and the loss of intraepidermal nerve fibers in the hind paw. Concomitant administration of SS-20 protected against the development of the neuropathy. Our results suggest that SS-20 may be a drug candidate for the prevention of CIPN.
引用
收藏
页码:1012 / 1018
页数:7
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